GeneSet Information

Tier III GS75619 • Transcripts Identified from Human Colitis Samples Using the 1300 Human cDNA Mini-Array

DESCRIPTION:

Comparison of data from both DNA microarray of mouse samples and cDNA mini-array of human biopsy samples is shown in Table 4. There are some similarities between the two analyses, but many changes in transcripts levels found from CD patients were not detected in TNBS treated mouse samples. A definitive conclusion could not be made in CD patients between the TNFa antibody treated and untreated groups due in part to the small sample sizes.

LABEL:

Hs.Colitis 1300MiniArray

SCORE TYPE:

Effect

DATE ADDED:

2010-06-22

DATE UPDATED:

2024-04-25

SPECIES:

AUTHORS:

Yamamoto S, Isuzugawa K, Takahashi Y, Murase Y, Iwata M, Arisawa T, Nakano H, Nishimura N, Yamato S, Ohta M, Ina K, Murata T, Hori M, Ozaki H, Imakawa K

TITLE:

Intestinal gene expression in TNBS treated mice using genechip and subtractive cDNA analysis: implications for Crohn's disease.

JOURNAL:

Biological & pharmaceutical bulletin Nov 2005, Vol 28, pp. 2046-53

ABSTRACT:

So far it has proven difficult to identify a causative gene(s) or gene product initiating the events that lead to inflammation of the intestinal mucosa and, ultimately, progression to Crohn's disease (CD), an inflammatory bowel disease. However, gene transcripts identified in the intestine of trinitrobenzene sulfonic acid (TNBS)-treated mice might suggest a clue, and even represent candidate genes leading to inflammation and mucosal damage, and to subsequent fibrosis. In the present study, DNA microarray (13000 transcripts) methodology was applied to mucosal RNA extracted from TNBS-treated mice, some transcripts of which were validated via cDNA subtraction and RT-PCR analyses. Intestinal biopsy samples from CD patients were then analyzed using cDNA mini-array (1300 cDNAs), focusing on gene transcripts associated with cancer and immunity. Mini-array results revealed transcript changes similar and also dissimilar to those found from the DNA microarray analysis. These changes, previously known or newly identified, possibly occurring during the initial and progressive stages of inflammatory conditions may provide a clue to identify marker transcripts and/or targets for the development of future gene therapy. PUBMED: 16272687
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Gene Therapy (D015316)
Fibrosis (D005355)
Animals (D000818)
RNA (D012313)
Forecasting (D005544)
Intestinal Mucosa (D007413)
Humans (D006801)
DNA (D004247)
Trinitrobenzenesulfonic Acid (D014302)
Immunity (D007109)
Mice (D051379)
Patients (D010361)
Microarray Analysis (D046228)
Neoplasms (D009369)
Intestines (D007422)
Reverse Transcriptase Polymerase Chain Reaction (D020133)
Oligonucleotide Array Sequence Analysis (D020411)
Inflammation (D007249)
Mice, Inbred C57BL (D008810)
Lead (D007854)
Colitis (D003092)
DNA, Complementary (D018076)
Inflammatory Bowel Diseases (D015212)
Crohn Disease (D003424)
Mucous Membrane (D009092)
Biopsy (D001706)
Sample Size (D018401)
intestine (MA:0000328)
bowel (MA:0001524)
colitis (MP:0002816)
fibrosis (MP:0003045)
abnormal inflammatory response (MP:0001845)
immunoglobulin complex, circulating (GO:0042571)
gene expression (GO:0010467)

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Supported by NIH R01 AA18776 jointly funded by NIAAA and NIDA, and JAX Center for Precision Genetics NIH U54 OD 020351